We have shown that the plasmas of patients with atopic asthma, and asthma secondary to aspirin or metabisulfite sensitivity have significantly elevated circulating levels of a heparin-like material (EHM). A diminution of trabecular bone not related to corticosteroid therapy has been reported in bone density measurements of asthmatics when compared to age- and sex-matched controls; this bone loss is substantially increased by corticosteroid therapy. It is known that large heparin dosages admninistered therapeutically or in experimental animals can produce osteopenia and crush fractures. The mechanism of heparin-induced osteopenia is unknown, but heparin has been shown to stimulate collagenase and parathyroid hormone activity, to inhibit calcitonin, an inhibitor of bone resorption, and in a recent study, to significantly lower the serum concentration of 1,25-dihydroxyvitamin D3 (calcitriol), the vitamin D3 metabolite, considered to be the most potent calcium regulator. Utilizing dual-photon absorptiometry, we plan to examine the trabecular bone density in a group of asthmatics and age- and sex-matched controls under the age of 45, to determine whether corelations can be established with circulating EHM levels. We will also assay serum indices of calcium and bone metbolism, including calcium, phosphorus, alkaline phosphatase, parathormone, calcitonin, 1,25-dihydroxyvitamin D, and bone GLa protein (BGP) and determine their correlation with EHM levels and bone density indices. It is hoped that an elucidation of our understanding of factors that may produce osteopenia in asthmatics prior to the initiation of corticosteroid therapy can contribute toward the development of measures that might control this process and thus diminish the sum total bone loss after corticosteroids.